Wyniki wyszukiwania

1

Cellular basis of extinction of conditioned fear and its renewal

100%

Knapska E.

Acta Neurobiologiae Experimentalis

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2011

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tom 71

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nr S

The memory of fear extinction is context-dependent: fear, suppressed in the extinction context, can renew in other contexts, invalidating the exposure therapy. Understanding the neuronal circuits underlying fear extinction is, therefore, of clinical relevance. Recent research suggests mediation of fear extinction by highly specific neuronal circuits in the amygdala, prefrontal cortex and hippocampus. However, at the cellular level, the interrelations between these brain structures remain unclear. Using c-Fos immunohistochemistry, we found strong suggestions that the context specificity of extinction is mediated by prefrontal modulation of amygdala activity and that the hippocampus has a crucial role in contextual memory retrieval. We then aimed at characterization of amygdala neurons involved in retrieval of extinguished fear memories. The use of recently generated transgenic rats carrying gene encoding fusion of PSD-95/Venus protein enabled us to study the connections of the activated neurons. The rats were injected with two anterograde axonal transport tracers either into the infralimbic (IL) and prelimbic (PRL) cortices or into the prefrontal cortex and ventral hippocampus (vHIPP). We showed that most of the cells activated in the lateral nucleus of the amygdala (La) by the extinction training receive inputs from the IL, whereas the neurons activated by the renewal of fear mainly receive signals from the PRL and vHIPP. Such differences were absent in the central nucleus of the amygdala. This suggests that extinction and renewal activate different subpopulations of neurons in the La, and that they can be distinguished by their connections to the IL, PRL and vHIPP. We also observed different involvement of the inhibitory neurons within the La following fear extinction and fear renewal. Taken together, these data suggest an appealing possibility of increasing fear extinction and preventing fear renewal by very specific manipulations of the neurons in the La.

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Badanie uczenia się i pamięci u szczurów i myszy

100%

Knapska E.

Annals of Warsaw University of Life Sciences - SGGW. Animal Science

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2011

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tom 48

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Central amygdala mediates social modulation of on-going behavior

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Knapska E.

Acta Neurobiologiae Experimentalis

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2017

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tom 77

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nr Suppl.1

Human empathy emerges over phylogeny from various behavioral precursors. One of the simplest is emotional contagion, i.e. sharing emotional states between individuals. Tuning one’s emotional state to that of another increases the probability of similar behavior, which thereby allows for a rapid adaptation to environmental challenges. Emotional contagion, commonly observed in animals, is well described at the behavioral level, but the neural circuits necessary for sharing emotions are not well understood. To study neural circuits underlying emotional contagion we have developed behavioral rat models of adult, same-sex social interactions that induce positive emotions, active fear and passive fear. The neural circuits in the central nucleus of the amygdala (CeA) are crucial for both appetitively and aversively motivated non-social behaviors. In the latter case the CeA mediates both active and passive defensive responses. To test the hypothesis that the neural circuits of the CeA are necessary for socially transferred emotions of different valence we used c-fos-driven targeting of channelrhodopsin and halorhodopsin to activate or inhibit neurons involved in social interactions. We show that activation of the CeA neurons involved in social interactions of different emotional valence in a novel environment resulted in distinct behavioral patterns. Activation of the CeA “positive” neurons increased exploration of the environment, activation of the “passive fear” neurons motivated rats to hide and activation of the “active fear” neurons enhanced risk assessment behavior. Inhibiting the CeA neurons led to opposite effects. Taken together, our results show that the neural circuits within the CeA control socially transmitted emotions and their impact on on-going behavior. Social emotions of different valence involve subpopulations of CeA neurons that are, at least partially, distinct. FINANCIAL SUPPORT: the National Science Centre grant 2013/11/B/NZ3/01560, European Research Council Starting Grant.

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Central amygdala mediates social modulation of on-going behavior

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Knapska E.

Acta Neurobiologiae Experimentalis

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2017

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tom 77

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nr Suppl.1

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Neuronal circuits in the central amygdala underlying emotional contagion

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Rokosz K., Knapska E.

Acta Neurobiologiae Experimentalis

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2015

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tom 75

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nr Supl.

BACKGROUND AND AIMS: Human empathy emerges over phylogeny from various behavioral precursors. One of the simplest is emotional contagion, i.e. sharing emotional states between individuals, which can be modelled in rodents. In our model of socially transferred fear we showed that a brief social interaction with a fearful cage mate (demonstrator) promotes aversive learning in an otherwise naïve rat (observer) and activates the amygdala of the observers, especially its central part (CeA). METHODS: To elucidate the role of neuronal circuits in the central amygdala of the observers, we used two methods of functional mapping: transgenic rats expressing in behaviorally activated neurons a PSD-95:Venus fusion protein and injected with anterograde tracer and a combination of retrograde tracing with c-Fos ISH. RESULTS: We have identified several afferent and efferent CeA projections active during socially transferred fear. We discovered strong activation especially in the periaqueductal gray (PAG) and dorsal raphe nuclei (DRN), structures receiving dense projections from the CeA and implicated in fear and anxiety disorders. Moreover, we observed that most of the activated cells are GABA-ergic neurons. To test whether the activated circuits are similar for the socially and non-socially induced emotions, we used double immunodetection for a PSD-95:Venus construct and endogenous c-Fos. About 70% of neurons was activated by both social interaction with fear conditioned partner and subsequent fear conditioning. Moreover, using optogenetics, we showed that specific activation of CeA neurons involved in socially transferred fear results in increased anxiety. CONCLUSIONS: These findings suggest that there exists a group of neurons in the central amygdala that is involved in integrating information about a threat, activated during socially transferred fear and subsequently recruited by learning of fear responses. Part of these cells is probably specifically involved in socially induced anxiety.

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Reciprocal patterns of c-fos expression in the medial prefrontal cortex and amygdala after extinction and renewal of conditioned fear in rats

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Knapska E., Maren S.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 3

Substantial evidence indicates that extinguished fear can be recovered after a change in experimental context (i.e., the renewal effect). The aim of this study was to characterize the neural circuitry underlying the retrieval of extinguished fear memories using c-Fos immunohistochemistry. Firstly, rats received auditory fear conditioning. Subsequently, they were extinguished by presenting CS-alone trials in either the same context as conditioning or in a second context. Then, all rats were tested for their fear of the auditory CS in the second context and sacrifi ced 90 min after testing. The presentation of the extinguished CS outside of the extinction context resulted in renewal of the freezing response relative to animals tested to the CS in the extinction context. In addition, the renewal of fear was associated with c-Fos expression in the prelimbic division of the medial prefrontal cortex, the lateral and basolateral nuclei of the amygdala, and the medial division of the central nucleus of the amygdala. In contrast, the presentation of the CS in the extinction context induced c-Fos expression in the infralimbic cortex, the intercalated nuclei of the amygdala and the dentate gyrus. Hippocampal areas CA1 and CA3 exhibited c-Fos expression when the CS was presented in either context. These data suggest that the context-specifi city of extinction may be mediated by prefrontal modulation of amygdala activity, and that the hippocampus may have a fundamental role in contextual memory retrieval.

7

Inhibition and activation of the central amygdala circuits involved in social interaction suppresses motivation for sucrose reward

63%

Rojek-Sito K., Knapska E.

Acta Neurobiologiae Experimentalis

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2019

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tom 79

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nr Suppl.1

INTRODUCTION: Appetitive motivation systems evolved to mediate a wide array of adaptive behaviors aimed at providing resources such as food or social contacts. AIM(S): The question whether motivation to approach various types of reward involves different neuronal mechanisms is still largely unanswered. In particular, it is not known whether neuronal circuits controlling social motivation are uniquely social, i.e., do they apply only to the social domain and are not utilized by other non‑social motivational processes? METHOD(S): To address this question, we manipulated activity of the central amygdala (CeA) circuits activated during either instrumental conditioning for food reward or interaction with a partner. CeA has been implicated in generating intense incentive motivation for food and drugs. Using c‑fos-driven targeting with halorhodopsin and channelorhodopsin, we were able to inhibit or activate the respective neuronal subpopulations in the CeA during the Skinner box session, in which motivation was assessed in the progressive-ratio schedule of food-pellet reinforcement. To obtain food pellets rats, had to press the lever. The number of responses required to get reinforced increased when the reward was obtained. Motivation was measured as the highest number of responses performed to obtain the food reward. RESULTS: We observed that both inhibition and activation of either the social or food neuronal circuits in the CeA resulted in significantly decreased motivation for sucrose reward; however, the pattern of behavioral responses observed after manipulation of sucrose- and social‑related neuronal circuits was different. CONCLUSIONS: The results suggest that social and food motivation depends on circuitsthat overlap only partially.

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Zaraźliwe emocje

63%

Rokosz E., Knapska E.

Wszechświat

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2014

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tom 115

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nr 01-03

9

Lack of matrix metalloproteinase 9 (MMP-9) affects LTP in the basal and central nuclei but not in the lateral nucleus of the amygdala

51%

Gorkiewicz T., Balcerzyk M., Kaczmarek M., Knapska E.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr Suppl.1

Matrix metalloproteinase-9 (MMP-9) is an extracellularly operating endopeptidase, which cleaves extracellular matrix proteins and plays an important role in synaptic plasticity, learning and memory. It is expressed in neurons in many different brain structures, including the hipocampus, prefrontal cortex and amygdala. MMP-9 is involved in maintenance of long-term potentiation (LTP) in the hipocampus and prefrontal cortex. On the other hand, its role in synaptic plasticity in the amygdala is much less known. It has been shown that the MMP-9 knock-out (MMP-9 KO) mice are impaired in amygdala-dependent appetitively motivated learning. The amygdaloid complex consists of several cytoarchitectonically and functionally distinguishable nuclei. To investigate MMP-9-dependent synaptic plasticity in different amygdalar nuclei, we studied MMP-9 role in LTP evoked in the central (CE), basal (BA) and lateral (LA) nuclei of the amygdala. In our in vitro extracellular recordings we used slices from MMP-9 KO and control mice. LTP in the BACE and LA-BA pathways was induced at the same level in the MMP-9 KO and control slices but it was disrupted several minutes after induction. In contrast, LTP in the external capsule-LA pathway was not disturbed in MMP-9 KO. These data suggests that MMP-9 is involved in stabilization but not in induction of LTP only in particular nuclei of the amygdala.

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Basolateral amygdala and hippocampal imputs to prefrontal cortex neurons, activated by high and low levels of fear

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Bukowczan J., Szadzinska W., Knapska E.

Acta Neurobiologiae Experimentalis

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2015

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tom 75

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nr Supl.

BACKGROUND AND AIMS: Fear extinction is a useful model for exposure-based therapies for the treatment of human anxiety disorders, such as phobias and posttraumatic stress disorder. Extinction of conditioned fear leads to formation of a new memory trace. Extinction memory is susceptible to the change of environment (context) in which conditioned stimulus (CS) is presented (promoting fear renewal), and to the passage of time (leading to spontaneous recovery of fear). Though the return of fear after extinction is a considerable challenge for the efficacy of exposure-based therapies, the neuronal basis of this phenomenon is not fully understood. METHODS: To understand better the neuronal bases of extinction memory, we characterize the amygdalar and hippocampal active projections to prefrontal cortex during retrieval of extinction memory. We use anterograde tracing in a transgenic rat in which neurons express a dendritically-targeted PSD-95:Venus fusion protein under the control of a c-fos promoter. Rats were subjected to auditory fear conditioning, followed by fear extinction and then presented to the extinguished CS in the extinction or fear conditioning context. RESULTS: Rats showed low levels of freezing when tested in the extinction context 24 hours after extinction and high levels of fear when tested in the conditioning context (either 24 hour or 28 days after extinction) or in the extinction context after 28 days (spontaneous recovery). The analysis of active projections shows that prefrontal cortex receives equal number of inputs from both basolateral amygdala and ventral hippocampus. However, the basolateral projections are dominant in neurons activated by high levels of fear. CONCLUSION: The obtained results suggest that basolateral inputs to the prefrontal cortex may drive retrieval of fear memory, as opposed to hippocampal inputs.

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Influence of chronic fluoxetine treatment on apetitive learning in matrix metalloproteinase-9 knock-out mice

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Charzewski L., Puscian A., Knapska E.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr Suppl.1

Matrix metalloproteinase-9 (MMP-9) is an extracellular endopeptidase which cleaves extracellular matrix proteins and plays a significant role in synaptic plasticity, learning and memory. Impairment of MMP-9 knock-out mice in appetitively motivated learning has been previously shown. In the present project we investigated whether chronic treatment with fluoxetine, antidepressant drug, which stimulates synaptic plasticity, would affect appetitive learning of MMP-9 knock-out mice. To this end, MMP-9 knock-out and wild type mice were treated with fluoxetine or vehicle for 35 days, and trained in sucrose-water discrimination task in the IntelliCage system. The IntelliCage system allows for long-term monitoring of the behavior of group-housed animals. For five days the mice had to discriminate between bottles (placed on two sides of the same corner of the cage) that contained either sweetened or plain water. The results suggest that chronic fluoxetine treatment improves appetitive learning of MMP-9 knock-out mice.

12

New and “cool” methods in behavioral neuroscience

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Boguszewski P. M., Puscian A., Knapska E.

Acta Neurobiologiae Experimentalis

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2014

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tom 74

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nr 3

Behavioral tests in laboratory rodents play an essential role in basic and applied biomedical research. Development of new animal models for neurological and psychiatric disorders, as well as preclinical phase of drug research require a „proof-of-concept” testing on a system level. Since most of the behavioral procedures are not rigorously standardized, it is difficult to obtain replicable results between laboratories. One of the approaches to solve this problem is designing more ethologically-relevant behavioral tasks, in which behavioral expression is more voluntary and manifold behavioral measures are collected over long periods. Collecting large amounts of data requires automatic control of all stages of a study – experimental cage/system manipulation, data gathering and analysis. Such automated systems offer important advantages. They increase level of standardization that results in more coherent data, save time and manpower, as well as reduce animal numbers required. Automated monitoring, although new and often sophisticated, could be cheap as well. The inspiration comes from growing popularity of amateur robotics, accessibility of 3D printing and progress in electronics. The aim of the lecture is to present new tests and solutions we are developing in Nencki Institute, including RFID tags for social experiments, automatic vocalization classification, video image animals detection and recognition software and even Mindstorm Lego robots.

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c‑Fos and neuronal plasticity: the aftermath of Kaczmarek’s theory

51%

Jaworski J., Kalita K., Knapska E.

Acta Neurobiologiae Experimentalis

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2018

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tom 78

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nr 4

The development of molecular biology methods in the early 1980s led to a better understanding of the role of transcription factors in mammalian cells. The discovery that some transcription factors are critically important for cells to switch between different functional states was fundamental for modern molecular neurobiology. In the 1980s Leszek Kaczmarek proposed that, analogically to the cell cycle or to cell differentiation, long‑term synaptic plasticity, learning, and memory should also require the activity of transcription factors. To test his hypothesis, he focused on c‑Fos. His team showed that the c‑Fos proto‑oncogene is activated by synaptic plasticity and learning, and is required for these phenomena to occur. Subsequent studies showed that timp‑1 and mmp‑9 are c‑Fos effector genes that are required for plasticity. The present review summarizes Kaczmarek’s hypothesis and the major evidence that supports it. We also describe the ways in which knowledge of the molecular neurobiology of learning and memory advanced because of Kaczmarek’s theory. Finally, we briefly discuss the degree to which his hypothesis holds true today after the discovery of non‑coding RNAs, a novel class of regulatory molecules that were not taken into account by Leszek Kaczmarek in the 1980s.

14

Neural circuits in the central amygdala mediate socially transferred fear

51%

Rokosz K., Hamed A., Kondrakiewicz K., Knapska E.

Acta Neurobiologiae Experimentalis

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2017

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tom 77

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nr Suppl.1

INTRODUCTION: Social complex behavior, like empathy, emerge over phylogeny from various precursors. One of the simplest is emotional contagion, i.e. sharing emotional states between individuals. Receiving signals of a potential danger may increase chances of survival, thus emotional contagion plays an important role in learning about external environment. The phenomenon is well described at the behavioral level, but the neural circuits necessary for sharing emotions are unknown. We designed a rat model of fear contagion and showed that a brief social interaction with a fearful cage mate promotes risk assessment behavior and activates the central amygdala (CeA) in an otherwise naïve rat. AIM(S): The purpose of this project was to elucidate the role of the CeA circuits involved in socially shared fear. METHOD(S): To investigate the functional outputs of the activated CeA neurons, we mapped neural circuits downstream from the CeA combining anterograde tracing with an imaging of activated neurons in transgenic “Venus” rats. To test the function of CeA “social fear” neurons, we optogenetically stimulated or inhibited subpopulation of CeA neurons activated by social interaction using c-fos-driven targeting of channelrhodopsin and halorhodopsin. RESULTS: In rats that socially shared fear of their partners, we observed strong activation of structures involved in anxiety and motor functions. Most of the activated cells received projections from the CeA. Optogenetic activation of the “social fear” neurons in a social context led to behavioral pattern resembling the one observed during social interaction with a fearful partner. Activation of neurons in non-social context induced exploration and risk assessment behavior (active fear). Inhibition of them had the opposite effects. CONCLUSIONS: The results suggest that the CeA neurons involved in socially transferred fear mediate active fear responses and anxiety-related behaviors in both social and non-social conditions.

15

Localization of recent and remote memory traces for successful and impaired fear extinction

51%

Szadzinska W., Rokosz K., Mikosz M., Knapska E.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr Suppl.1

Extinction of conditioned fear leads to formation of a new memory trace. There are, however, factors altering behaviors associated with such a memory trace, such as CS presentation outside the extinction context (promoting fear renewal) and re-emerging of fear with the passage of time after extinction (spontaneous recovery). The neuronal basis of these phenomena is poorly understood. The involvement of hippocampal-prefrontal cortical circuits was investigated only during initial processing of fear extinction memory. As has been shown before for fear conditioning, the mechanisms underlying matured memory may differ from those of recent memory. In our study we used c-Fos immunohistochemistry to generate a functional map of the neural circuits involved in contextual retrieval of recent and remote memories of extinguished fear. Presentation of the CS in the extinction context 24 h after extinction yielded low freezing and induced strong activation of infralimbic cortex (IL) and ventral hippocampus (vHIPP). Similar presentation after 28 days resulted in high freezing and much lower activity of IL and vHIPP. In contrast, presentation of the CS outside the extinction context after either 24 h or 28 days yielded high freezing and induced strong activation of prelimbic cortex. These results suggest remodelling of the fear extinction memory trace over time, as well as dissociable neuronal mechanisms underlying fear renewal and spontaneous recovery.

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Prefrontal cortex single unit activity during extinction of conditioned fear

51%

Szadzinska W., Jercog D., Knapska E., Herry C.

Acta Neurobiologiae Experimentalis

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2017

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tom 77

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nr Suppl.1

INTRODUCTION: In fear extinction, a model of exposure-based therapy, a tone-conditioned stimulus previously paired with a footshock is presented repeatedly in the absence of the aversive outcome, resulting in fear reduction. It is well documented that the dorsal (including the prelimbic area, PL) and the ventral (the infralimbic area, IL) regions of the medial prefrontal cortex (mPFC) differentially regulate conditioned fear responses. The PL stimulation increases, whereas the IL stimulation decreases fear expression. In addition, the IL is critical for consolidation of extinction memories. Little is known, however, how different parts of the prefrontal cortex interact with each other and how their activity changes in the course of the extinction training. AIM(S): We aimed at detailed description of neural activity changes within the PL and IL during fear extinction. METHOD(S): We performed single unit recordings simultaneously in the PL and IL, during the habituation and two sessions of fear extinction in freely moving mice. Recorded neurons were divided into excitatory pyramidal cells and interneurons. The neuronal responses to the conditioned stimuli were analyzed and the activity of significantly responsive neurons was averaged. RESULTS: We found patterns of the single unit activity that differed along the dorso‑ventral axis of the mPFC. The averaged IL activity followed the behavior during the extinction session, while the PL pronouncedly showed inhibition during the fear expression at the beginning of the extinction session but not at later times. CONCLUSIONS: The results suggest different involvement of the PL and IL during the acquisition of extinction association, with the PL being mostly active during the high fear state, while the IL being active throughout the entire extinction session. The analysis of the mPFC activity suggests that its ventral region is mostly involved in the change of the association value from the perceiving conditioned stimuli as a threatful to the point of perceiving it as safe. FINANCIAL SUPPORT: ERC.

17

Zarazić się strachem

51%

Kaczmarek L., Knapska E., Werka T.

Świat Nauki

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2007

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nr 07

18

New measures of social interactions for ecoHAB cage

51%

Maka J., Puscian A., Knapska E., Wojcik D. K.

Acta Neurobiologiae Experimentalis

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2017

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tom 77

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nr Suppl.1

INTRODUCTION: Eco-HAB is an open source system for automated measurements and analysis of social preferences and in-cohort sociability in mice. It requires no contact between a human experimenter and tested animals. In Eco-HAB, group-housed mice live in a spacious, four-compartment, resembling natural burrows. It allows an assessment of the tendency of mice to voluntarily spend time together in ethologically relevant mouse group sizes. Results are obtained faster, with less manpower needed and without confounding factors. AIM(S): The aim of the of this study is to develop measures for the EcoHAB system, which could well describe social relations in a group of mice. We test the proposed measures in experiments with four FX WT and three FX KO groups. We expected that FX KO mice would have disturbed social skills comparing to FX WT. METHOD(S): We developed a dedicated workflow for analysis of social interactions based on analysis of the decision patterns. For each pair of mice, one mouse is a leader, the other is a follower. After the leader changes the room, the follower’s reaction in a 3-second window is analysed. If the follower acts on the leader’s movement and follows it, the pattern is classified as “following”; otherwise it is “evasion”. Lack of follower’s reaction is ignored. The numbers of interactions for each pair and distribution of the patterns were obtained. To characterize the relations between the mice in selected time windows we used binomial model. We also studied changes of these relation in time and their distribution in mice groups. RESULTS: Our study proved that FX KO mice have significantly less interactions within a pair than FX WT. What’s more, FX WT are following each other more often and the character of interaction is more stable. CONCLUSIONS: EcoHAB is a good environment for conducting advanced analysis of mice social interactions. Proposed measures show significant difference between WT and KO group and are a promising tool to study social interactions.

19

Highly replicable, fully automated measures of perseverative behaviors in Intellicage system

51%

Puscian A., Leski S., Romanowska A., Knapska E.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr Suppl.1

Perseveration, defined as resistance to change in routine and repetitive behaviors, is one of the core symptoms of Autism Spectrum Disorders. It was proposed that an inability to break habits, experienced by autistic people, corresponds, in animal models, to impaired performance in the learning tasks that assess ability to change a response strategy to obtain reinforcement. However, the results of conventional behavioral tests can be confounded by anxiety related to handling and social isolation. In order to avoid such effects and to analyze phenotypes of subjects in an efficient manner, we developed a battery of automated tests aimed at appraising behavioral flexibility in mice. The tests were performed in the IntelliCage (IC), a computer-controlled system, which can be used for long-term monitoring of group-housed animals. These tests allow for measuring of exploration patterns, pace and progress of appetitive and reversal learning. To standardize and evaluate the relevant IC tests, we compared valproate treated and control animals from two inbred strains of mice, C57BL/6 and BALB/c. We show that tested mice differ significantly in most of the examined parameters. The obtained results are highly replicable between tested cohorts of subjects, thereby allowing us to infer, that the reported battery of automated behavioral and cognitive tests is a valuable tool in verifying suitability of mouse models of ASD symptoms.

20

Social modulation of conditioned fear extincion in mice

51%

Nowak A., Werka T., Knapska E.

Acta Neurobiologiae Experimentalis

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2011

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tom 71

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nr S

Fear-eliciting properties of a stimulus acquired through conditioning can be extinguished by repeatedly presenting the conditioned stimulus (CS) in the absence of the unconditioned stimulus. Such extinction process does not reflect unlearning of the original association, but results in a transient inhibition of fear. For example, extinguished fear responses may return after a change in context (i.e., renewal). The return of fear after extinction is a considerable challenge for maintaining long-lasting fear suppression after exposure-based therapies. Until recently, the recovery phenomena were studied only in isolated animals. Social context is an important factor affecting behavior of the animals extensively interacting with their conspecifics, such as humans and mice. In the present study, we examined the influence a conspecific behavior on renewal of extinguished fear. Male C57BL/6 mice were housed in pairs, handled in order to minimize stress caused by the experimenter’s presence, and then separately subjected to cued fear conditioning. Subsequently, one mouse of the pair was subjected to 6 sessions of fear extinction that significantly reduced the conditioned response (freezing) to the CS. Another mouse from the pair was merely exposed to the experimental cage for equivalent amount of time, therefore its freezing to the CS remained high. On the test day, the mice were tested either together or separately. The animals were trained and tested in a two-compartment cage, which was divided by a perforated transparent partition allowing the mice to see, hear and smell their neighbor, but not to contact them physically. We report that exposure to a fearful familiar conspecific results in renewal of conditioned fear in a mouse that was previously subjected to successfull extinction procedure. The animal model presented here can be a useful tool for studying neuronal basis of the social aspects of fear recovery after extinction.

Ograniczanie wyników

Cellular basis of extinction of conditioned fear and its renewal

Badanie uczenia się i pamięci u szczurów i myszy

Central amygdala mediates social modulation of on-going behavior

Central amygdala mediates social modulation of on-going behavior

Neuronal circuits in the central amygdala underlying emotional contagion

Reciprocal patterns of c-fos expression in the medial prefrontal cortex and amygdala after extinction and renewal of conditioned fear in rats

Inhibition and activation of the central amygdala circuits involved in social interaction suppresses motivation for sucrose reward

Zaraźliwe emocje

Lack of matrix metalloproteinase 9 (MMP-9) affects LTP in the basal and central nuclei but not in the lateral nucleus of the amygdala

Basolateral amygdala and hippocampal imputs to prefrontal cortex neurons, activated by high and low levels of fear

Influence of chronic fluoxetine treatment on apetitive learning in matrix metalloproteinase-9 knock-out mice

New and “cool” methods in behavioral neuroscience

c‑Fos and neuronal plasticity: the aftermath of Kaczmarek’s theory

Neural circuits in the central amygdala mediate socially transferred fear

Localization of recent and remote memory traces for successful and impaired fear extinction

Prefrontal cortex single unit activity during extinction of conditioned fear

Zarazić się strachem

New measures of social interactions for ecoHAB cage

Highly replicable, fully automated measures of perseverative behaviors in Intellicage system

Social modulation of conditioned fear extincion in mice